Journal of Pediatric Ophthalmology and Strabismus

Downgaze Restriction After Placement of Superior Oblique Tendon Spacer for Brown Syndrome/Discussion

M Edward Wilson, MD; Robbin B Sinatra, MD; Richard A Saunders, MD; Arthur Jampolsky, MD

Abstract

M. Edward Wilson, MD, Robbin B. Sinatra, MD, and Richard A. Saunders, MD

ABSTRACT

Diplopia in the reading position developed in two patients with unilateral Brown syndrome after a 7millimeter section of #240 silicone retinal band was sewn between the cut ends of the superior oblique tendon at tenotomy. In both cases, forced auctions were positive, indicating a restrictive downgaze deficit. Surgical exploration revealed adhesions that prevented the normal sliding of the superior oblique tendon beneath the superior rectus muscle. Forced ductions became normal and downgaze improved after removal of the silicone band. Secondary superior oblique muscle paresis was also evident at the time of reoperation, requiring recession of the contralateral inferior rectus muscle (cases 1 and 2} and recession of the ipsilateral inferior oblique muscle (case 1). A restrictive downgaze deficit and a pareti e over-correction must be recognized as possible complications of the superior oblique tendon silicone "expander" operation.

INTRODUCTION

Brown syndrome, originally named the superior oblique tendon sheath syndrome, is a well-recognized ocular motility disorder characterized most notably by limitation of elevation in adduction.1 The cause is recognized now to be a restriction of free passage of the superior oblique tendon through the trochlear complex.2 Because the trochlear "pulley" is relatively inaccessible, surgical treatment is directed toward lengthening a presumably innocent structure, the superior oblique tendon. Because superior oblique muscle overaction is rarely present in Brown syndrome, superior oblique tendon lengthening can lead to ipsilateral inferior oblique muscle overaction and other signs superior oblique muscle palsy.

Tenotomy of the superior oblique tendon adjacent to the nasal border of the superior rectus muscle has become the most common operation to treat Brown syndrome. In spite of attempts to leave the intermuscular septum largely intact, secondary superior oblique muscle palsy still develops in 20% or more of patients over time.3 Simultaneous ipsilateral inferior oblique muscle recession and superior oblique tendon tenotomy can reduce the risk of inferior oblique muscle overaction postoperatively, but the improvement in ocular elevation deficiency is slowed.4

In an attempt to produce a controlled lengthening of the superior oblique tendon with early normalization of ductions but no superior oblique muscle palsy, Wright5 described the use of a silicone "expander.* In this operation, a section of #240 silicone band is sewn between the cut ends of the superior oblique tendon following tenotomy performed nasal to the superior rectus muscle. Based on surgical results in three patients with follow up of 6 months to 4 years, Wright et al6 recommended the silicone expander operation as the procedure of choice for Brown syndrome. We report, herein, two patients in whom diplopia in the reading position developed after oblique tendon tenotomy and placement of a silicone spacer for unilateral Brown syndrome. In to a restrictive downgaze deficit, both of our patients also showed evidence of superior oblique muscle palsy by the time of reoperation.

CASE REPORTS

Case 1. Brown syndrome of the right eye developed in a 37-year-old woman after endoscopie sinus surgery. A left face turn and a slight chin-up posture were maintained to avoid diplopia. Elevation in adduction of the right eye was markedly reduced, and a downshoot was present in left gaze, but no underaction or overaction of the superior oblique muscles were present (Fig 1). Oral nonsteroidal antiinflammatory medications, oral corticosteroide, and a corticosteroid injection into the region of the trochlea did not improve her ocular motility. Because of persistent troublesome diplopia, especially in right gaze and up gaze, the patient requested surgical intervention. Her preoperative diplopia visual field is shown in Figure 2 (left).

In both case 1 and case 2, the early postoperative results…

M. Edward Wilson, MD, Robbin B. Sinatra, MD, and Richard A. Saunders, MD

ABSTRACT

Diplopia in the reading position developed in two patients with unilateral Brown syndrome after a 7millimeter section of #240 silicone retinal band was sewn between the cut ends of the superior oblique tendon at tenotomy. In both cases, forced auctions were positive, indicating a restrictive downgaze deficit. Surgical exploration revealed adhesions that prevented the normal sliding of the superior oblique tendon beneath the superior rectus muscle. Forced ductions became normal and downgaze improved after removal of the silicone band. Secondary superior oblique muscle paresis was also evident at the time of reoperation, requiring recession of the contralateral inferior rectus muscle (cases 1 and 2} and recession of the ipsilateral inferior oblique muscle (case 1). A restrictive downgaze deficit and a pareti e over-correction must be recognized as possible complications of the superior oblique tendon silicone "expander" operation.

INTRODUCTION

Brown syndrome, originally named the superior oblique tendon sheath syndrome, is a well-recognized ocular motility disorder characterized most notably by limitation of elevation in adduction.1 The cause is recognized now to be a restriction of free passage of the superior oblique tendon through the trochlear complex.2 Because the trochlear "pulley" is relatively inaccessible, surgical treatment is directed toward lengthening a presumably innocent structure, the superior oblique tendon. Because superior oblique muscle overaction is rarely present in Brown syndrome, superior oblique tendon lengthening can lead to ipsilateral inferior oblique muscle overaction and other signs superior oblique muscle palsy.

Tenotomy of the superior oblique tendon adjacent to the nasal border of the superior rectus muscle has become the most common operation to treat Brown syndrome. In spite of attempts to leave the intermuscular septum largely intact, secondary superior oblique muscle palsy still develops in 20% or more of patients over time.3 Simultaneous ipsilateral inferior oblique muscle recession and superior oblique tendon tenotomy can reduce the risk of inferior oblique muscle overaction postoperatively, but the improvement in ocular elevation deficiency is slowed.4

In an attempt to produce a controlled lengthening of the superior oblique tendon with early normalization of ductions but no superior oblique muscle palsy, Wright5 described the use of a silicone "expander.* In this operation, a section of #240 silicone band is sewn between the cut ends of the superior oblique tendon following tenotomy performed nasal to the superior rectus muscle. Based on surgical results in three patients with follow up of 6 months to 4 years, Wright et al6 recommended the silicone expander operation as the procedure of choice for Brown syndrome. We report, herein, two patients in whom diplopia in the reading position developed after oblique tendon tenotomy and placement of a silicone spacer for unilateral Brown syndrome. In to a restrictive downgaze deficit, both of our patients also showed evidence of superior oblique muscle palsy by the time of reoperation.

CASE REPORTS

Case 1. Brown syndrome of the right eye developed in a 37-year-old woman after endoscopie sinus surgery. A left face turn and a slight chin-up posture were maintained to avoid diplopia. Elevation in adduction of the right eye was markedly reduced, and a downshoot was present in left gaze, but no underaction or overaction of the superior oblique muscles were present (Fig 1). Oral nonsteroidal antiinflammatory medications, oral corticosteroide, and a corticosteroid injection into the region of the trochlea did not improve her ocular motility. Because of persistent troublesome diplopia, especially in right gaze and up gaze, the patient requested surgical intervention. Her preoperative diplopia visual field is shown in Figure 2 (left).

FIGURE 1: Preoperative gaze composite from case 1, There is a limitation of elevation in adduction in the right eye. Downgaze is normal.

FIGURE 1: Preoperative gaze composite from case 1, There is a limitation of elevation in adduction in the right eye. Downgaze is normal.

FIGURE 2: Diplopia fields from case 1. On the left is the diplopia visual field 4 weeks after the placement of the Bilicane spacer. At 12 weeks following placement of the silicone (center), note worsening of the diplopia visual field. On the right, improvement of the diplopia visual field after removal of the silicone and surgery for right superior oblique muscle palsy.

FIGURE 2: Diplopia fields from case 1. On the left is the diplopia visual field 4 weeks after the placement of the Bilicane spacer. At 12 weeks following placement of the silicone (center), note worsening of the diplopia visual field. On the right, improvement of the diplopia visual field after removal of the silicone and surgery for right superior oblique muscle palsy.

Four months after injury, the patient was taken to the operating room where a right superior oblique tendon tenotomy with insertion of a 7-millimeter section of a #240 silicone band was performed nasal to the superior rectus muscle. A superior temporal fornix incision was used and intermuscular septum was left intact along the nasai border of the superior rectus muscle. The silicone spacer was placed 3 mm medial to the superior rectus muscle as recommended by Wright.7 Care was taken to avoid contact with bare sclera beneath the superior oblique tendon at the surgical site. Forced ductions were positive at the onset and free at the conclusion of surgery. The intermuscular septum was not closed with suture over the spacer.

Six days postoperatively, the patient reported improvement in her field of single binocular vision. There was no spontaneous torticollis. Elevation in adduction was almost normal with only a mild residual Brown syndrome remaining. Downgaze was full. However, on examination 4 weeks later, the patient reported vertical diplopia in the reading position. Duction testing in the right eye revealed a downgaze deficit in both abduction and adduction (Fig 3). In addition, a right hyperphoria in the primary position and a positive Bielschowsky head tilt test were suggestive of a mild, right superior oblique muscle palsy (see gaze measurements - Fig 4). Two months postoperatively, diplopia had worsened and was now present intermittently even in the primary position. Findings of both superior oblique muscle palsy and a downgaze deficit were evident. Her postoperative diplopia visual field is shown in Figure 2 (center).

Three months after her first strabismus operation, repeat surgery was performed. Forced ductions were normal to elevation but verified a downgaze restriction in the right eye. Surgical exploration revealed adhesions between the silicone spacer and the nasal border of the superior rectus muscle (Fig 5). Forced ductions became normal after dissection and removal of the silicone spacer. The superior oblique tendon was not reconnected. Removal of the spacer thus resulted in a free tenotomy. In addition, the right inferior oblique muscle was recessed 10 mm and the left inferior rectus muscle was recessed 3 mm. Postoperatively, the patient's field of single binocular vision was greatly improved (Fig 2, right). She reported no diplopia in or near the primary position. Her postoperative result has remained stable over 12 months (see gaze measurements - Fig 4).

FIGURE 3: Case 1, 4 weeks postoperatively. The Brown syndrome in the right eye has resolved, but there is limitation of depression in both abduction and adduction.

FIGURE 3: Case 1, 4 weeks postoperatively. The Brown syndrome in the right eye has resolved, but there is limitation of depression in both abduction and adduction.

Case 2. An 11-year-old girl was referred for evaluation of Brown syndrome in the left eye. Her parents reported seeing an ocular misalignment in upgaze since infancy. The patient described an inability to move the left eye upward each day on awakening. The Brown syndrome would, at times, become intermittent later in the day, although over the preceding few months the intermittence had become much less frequeat. She also reported discomfort localized to the superior nasal orbit when attempting to elevate her left eye. A magnetic resonance imaging scan of the orbit was normal.

At the time of initial examination, a 15-degree chin-up posture was needed to maintain fusion and avoid diplopia. Elevation in adduction of the left eye was markedly limited. A downshoot of the left eye was also present in adduction (Fig 6). Oral antnnflammatory medications and corticosteroid injection to the region of the trochlea were refused. Observation and range of motion eye movements to tolerance were recommended. Over the next several months, the Brown syndrome became constant. Complaints of double vision increased and the chin-up posture became more evident to the parents. A left hypotropia of 12 prism diopters was present in forced primary gaze. A left superior oblique tenotomy with insertion of a 7-millimeter sik'cone spacer sewn to the cut-ends of the superior oblique tendon was, therefore, performed.

Six days postoperatively, she was orthophoric in primary gaze with no spontaneous head posturing. Although elevation was improved, a moderate residual Brown syndrome was present. Downgaze was full in adduction and abduction. Three weeks later, a downgaze deficit was present in both abduction and adduction. However, a 3-prism-diopter left hyperphoria in the primary position also suggested the presence of a superior oblique muscle palsy.

Eight and a half months after placement of the silicone spacer, the family requested another operation.

Intermittent double vision was present in the primary position and right gaze with constant diplopia in downgaze (Fig 7). The patient reported that she needed to bring reading material up into the primary position or depress her chin to avoid double vision. Stereopsis was maintained at 40 seconds of arc in upgaze. Intraoperative forced auctions were positive for a restrictive, downgaze deficit in the left eye. Forced auctions normalized after dissection and removal of the silicone expander, converting the surgery to a free tenotomy of the superior oblique tendon. A 2-millimeter recession of the right inferior rectus muscle was also performed because a small consecutive left hyperphoria was present in primary gaze. Postoperatively, the patient was orthophoric in the primary position, but a residual, intermittent, left hypertropia of 16 ? is present in downgaze. If further surgery is elected, placement of a posterior fixation suture on the right inferior rectus may be needed to match the residual downgaze deficit of the left eye.

DISCUSSION

The superior oblique expander operation is a novel concept first reported by Wright in 1991.5 He attempted to produce a graded elongation of the superior oblique tendon with functional preservation of its fanned-out insertion on the globe. Wright8 has recognized the potential for complications if the silicone expander scars to the underlying sclera, which could defeat the purpose of the expander and cause downgaze problems similar to those seen with superior oblique tendon recession. To avoid this complication, the temporal fornix conjunct! val approach as described by Parks,9 with careful unroofing of the superior oblique intermuscular septum, was recommended. For the treatment of unilateral Brown syndrome, Wright et al6 have compared the results of simultaneous superior oblique tendon tenotomy and inferior oblique muscle recession in four patients with the superior oblique tendon expander procedure in three patients. The silicone expander procedure was deemed superior because early undercorrections were found less commonly than with simultaneous superior oblique tendon tenotomy and inferior oblique muscle recession. However, this comparison may be misleading because simultaneous superior oblique tendon and inferior oblique muscle surgery commonly produce early undercorrection that improves slowly over time.4 Perhaps with longer follow up, the surgical results would have been more equal. While no patient in either group developed a consecutive superior oblique muscle palsy during the reported follow up, patients from both groups may eventually develop this complication. Four years of follow up were reported after the silicone expander procedure for Brown syndrome without development of superior oblique muscle palsy, but only in one patient. Significantly, Wright has reported no instances of downgaze deficiency.

Table

FIGURE 4: Postoperative gaze measurements from case 1.At 4 and 12 weeks after placement of the 7-millimeter spacer, there are findings suggestive of a superior oblique muscle palsy, as well as a downgaze deficit. Jen weeks after removal of the silicone, and right inferior oblique recession 10.0 mm and left inferior rectus recession 3.0 mm, there is improvement of the right hypertropia. XT = exotropia; X = exophoria; LH = left hyperphoria; RH - right hyperphoria; RHT = right hypertropia; LHT = left hypertropia.

FIGURE 4: Postoperative gaze measurements from case 1.At 4 and 12 weeks after placement of the 7-millimeter spacer, there are findings suggestive of a superior oblique muscle palsy, as well as a downgaze deficit. Jen weeks after removal of the silicone, and right inferior oblique recession 10.0 mm and left inferior rectus recession 3.0 mm, there is improvement of the right hypertropia. XT = exotropia; X = exophoria; LH = left hyperphoria; RH - right hyperphoria; RHT = right hypertropia; LHT = left hypertropia.

FIGURE 5: Surgeon's view, intraoperative photo of the removal of the silicone in case 1. Adhesions are present between the nasal border of the superior rectus muscle and the silicone (arrow).

FIGURE 5: Surgeon's view, intraoperative photo of the removal of the silicone in case 1. Adhesions are present between the nasal border of the superior rectus muscle and the silicone (arrow).

Prieto-Diaz10 has described limitation of depression in abduction, much like our two patients, after superior oblique tendon recession. This complication may be caused by reattachment of superior oblique tendon fibers anterior to the equator of the globe, changing the superior oblique muscle function from a depressor to an elevator. Lingua11 reports that adhesions between the superior oblique tendon and the nasal border of the superior rectus muscle can cause a restrictive downgaze deficit after superior oblique tendon recession and cautions that this also could be a complication of the superior oblique tendon expander procedure. Posterior sliding of the superior oblique tendon along the nasal border of the superior rectus muscle is necessary for complete depression. Ipsilateral superior rectus muscle contracture also can result in restrictive downgaze deficit, but this occurs only in long-standing superior oblique muscle paresis.

A restrictive downgaze deficit, verified by forced ductions and signs suggestive of secondary superior oblique muscle paresis, developed in our two patients after the silicone expander operation was performed for unilateral Brown syndrome. Although our patients were in some respects atypical (Brown syndrome after sinus surgery and a congenital intermittent Brown syndrome that became constant), there was no indication preoperatively that they would have responded to surgery differently than more typical, congenital constant Brown syndrome patients. Surgical indications were diplopia and abnormal head posturing in both cases.

FIGURE 6: Gaze composite photographs from case 2 before placement of the silicone spacer. Note limitation of elevation in adduction in the left eye. Dawngaze is normal preoperatively.

FIGURE 6: Gaze composite photographs from case 2 before placement of the silicone spacer. Note limitation of elevation in adduction in the left eye. Dawngaze is normal preoperatively.

FIGURE 7: Gaze composite photos of case 2, 4 weeks postoperatively. There is resolution of the Brown syndrome in the left eye, but there is limitation of depression of the left eye in both adduction and abduction.

FIGURE 7: Gaze composite photos of case 2, 4 weeks postoperatively. There is resolution of the Brown syndrome in the left eye, but there is limitation of depression of the left eye in both adduction and abduction.

In both case 1 and case 2, the early postoperative results were good. Downgaze diplopia began to appear 3 to 4 weeks after surgery along with evidence of superior oblique muscle palsy. At reoperation, adhesions were present between the superior oblique tendon and the nasal border of the superior rectus muscle. These adhesions appeared to interfere with the posterior sliding of the superior oblique tendon beneath the superior rectus muscle that is needed for full downgaze. Only a minimal amount of adhesion of the silicone spacer to the sclera was present in case 1, and no scierai adhesions were noted in case 2. We had been careful to avoid unnecessary disruption of the intermuscular septum along the nasal border of the superior rectus muscle and the intermuscular septum beneath the superior oblique tendon was preserved to prevent direct contact of the silicone with sclera. These surgical maneuvers are routine for the authors when performing conventional superior oblique tenotomy, even when a silicone spacer is not being used. With the exception of the suture closure of the intermuscular septum over the spacer, we attempted to adhere to Wright's7 procedural recommendations. Perhaps with the superior rectus muscle pulled temporally on the muscle hook during surgery, we did not achieve the fiali 3-millimeter separation of the spacer from the superior rectus border. However, we have now examined a third Brown syndrome patient with deficient downgaze after placement of a 7-millimeter #40 silicone band between the cut-ends of the superior oblique tendon. All procedural recommendations7 were followed, including suture closure of the intermuscular septum over the spacer. Forced duction testing was not done.

While we are concerned now about performing silicone spacer surgery unuaterally, we have performed the procedure bilaterally on eight patients with bilateral superior oblique muscle overaction. No patient in this bilateral group has a symptomatic downgaze deficit. Unlike patients with Brown syndrome, patients with ?* pattern strabismus and superior oblique muscle overaction usually have wellestablished suppression allowing a small induced hypertropia in downgaze to be asymptomatic. In addition, a downgaze deficit is more likely to escape detection on version testing if it is present bilaterally. Secondary superior oblique muscle palsy, present in both of our Brown syndrome patients, is also much less likely to occur when superior oblique tenotomy is performed for superior oblique muscle overaction. Because we performed corrective surgery for superior oblique muscle palsy coincident with removing the silicone spacer, the contribution of each to the improvement in alignment and auctions cannot be assessed accurately.

The superior oblique tendon expander procedure is now an established option in the surgical management of Brown syndrome or superior oblique muscle overaction. Whether restrictive downgaze deficit can be prevented by meticulous surgical technique remains uncertain. In addition, it is evident from our reported cases that an overcorrection suggestive of a secondary superior oblique muscle palsy may occur in some cases.

REFERENCES

1. Brown HW. Congénital structural anomalies. In: Alan JH, ed. Strabismus Ophthalmic Symposium I. St Louis, Mo: CV Moaby Company; 1950:205-236.

2. Wilaon ME, Eustis HS, Parks MM. Brown's syndrome. Surv Ophthalmol. 1989;34: 153-172.

3. Parks MM. Surgery for BrownÎ syndrome. In: Symposium on Strabismus. Transactions of the New Orleans Academy of Ophthalmology. St Louie, Mo: CV Mosby; 1978:157-177.

4. Parks MM, Eustis HS. Simultaneous superior oblique tenotomy and inferior oblique recession in Brown's syndrome. Ophthalmology. 1987;94: 1043- 1048.

5. Wight KW. Superior oblique silicone expander for Brown's syndrome and superior oblique overaction. J Pediatr Ophthalmol Strabismus. 1991 ;28: 101-107.

6. Wright KW, Min BM, Park C. Comparison of superior oblique tendon expander to superior oblique tenotomy for the management of superior oblique overaction and Brown syndrome. J Pediatr Ophthalmol Strabismus. 1992;29:92-97.

7. Wright KW. Color Atlas of Ophthalmic Surgery: Strabismus. Philadelphia, Pa; JB Lippincott; 1993:201-216.

8. Wright KW. Surgical management of superior oblique overaction and Brown's syndrome. Ophthalmology Clinics of North America. 1992; 5:67-78.

9. Parks MM. Atlas of Strabismus Surgery. Philadelphia, Pa: Harper and Row; 1983:191-195.

10. Prieto-Diaz J. Superior oblique overaction. Int Ophthalmol Clin. 1989;29:43-50.

11. Lingua RW. Comparison of superior oblique tendon expander to superior oblique tenotomy for the management of superior oblique overaction in Brown's syndrome: discussion. J Pediatr Ophthalmol Strabismus. 1992;29:98-99.

From the Storm Eye Institute, Medical University of South Carolina, Charleston, SC.

Dr Sinatra is currently with the Department of Ophthalmology, Vanderbilt School of Medicine, Nashville, Tenn.

Supported in part by an unrestricted grant to the Storm Eye Institute from Research to Prevent Blindness, Ine, New York, NY.

Reprint requests should be addressed to M. Edward Wilson, MD, Department of Ophthalmology, Medical University of South Carolina, 171 AshleyAve, Charleston, SC 29425.

Discussion

Arthur Jampolsky, MD

I want to thank the authors for allowing me to see the manuscript quite in advance of the meeting. I congratulate Dr Sinatra et al for their excellent presentation. It is with some trepidation that I offer a critique of the paper presented by Dr Sinatra, since I am well aware that this Palm Springs AAPO&S meeting is in their territory. Since I do not wish to incur any more bodily derangements than I already carry, I shall, with unaccustomed mildness, carefully discuss this presentation by Dr Sinatra.

I would like to address three points: 1) the difference between true Brown syndrome and a "Brown plus" condition, 2) complications of the tendon spacer procedure, and 3) differential diagnosis of superior oblique palsy and superior rectus contracture syndrome.

The authors present two cases which are not true Brown syndrome. Rather they are a Brown plus, ie, either/or a vertical in the primary position and head turn with chin-up compensatory position. A true Brown syndrome has no deviation in any of the horizontal positions of gaze nor in downgaze. All the difficulties are above the horizontal plane, and the limited upward movement forms a straight line demarcation with up and out rotation being normal. This is a most important distinction to make. The authors indicate that the "silicone expander operation was performed for unilateral Brown syndrome. Although our patients were in some respects atypical..." Neither of these patients had Brown syndrome and indeed they were very atypical and may lead to an unfortunate interpretation by others that what is being discussed is an operation for Brown syndrome.

Relative to indications for surgery, one must be careful to avoid translating indications for surgery and results in patients who do have a vertical deviation not only in their primary position, but in other horizontal gazes, and also may have an anomalous head position. The tendon expander surgical procedure does indeed produce a vertical in the primary position, and in a patient with true Brown syndrome there is a trade OOm no deviation in the primary for an induced vertical deviation. Hardly a good risk/ reward relationship.

The authors do a service by discussing the complications of restricted downgaze (in whatever case) that may occur as a result of this procedure. The postoperative restriction to downgaze, as evidenced by forced traction testing during surgery, more probably indicates a secondary contracture of the superior rectus, in the opinion of this discussant. Figure 3 depicts a deficient down and out rotation of the involved eye, with a yoke overaction of the opposite superior oblique muscle, without a V-eso pattern in downgaze, all supportive of the diagnosis of superior rectus contracture. The authors state that weeks postoperatively, "a right hyperphoria in the primary position and a positive Bielschowsky head tilt test were suggestive of a mild, right superior oblique muscle palsy." It should be recognized that the same findings are part of the superior rectus contracture syndrome.

To correct the surgically induced vertical in the important reading position, the expander was removed, "converting the surgery to a free tenotomy of the superior oblique tendon." Such a result is hardly a graded superior oblique weakening procedure, the intent of the tendon expander procedure. Additionally, to remedy the induced downgaze reading defect in the reported patients, the opposite eye's inferior rectus muscle was operated on in both cases, and additionally, in one case, the opposing inferior oblique muscle was recessed. And further, in one case, there was still a residual hyper in the downgaze position and further surgery was contemplated. The authors wisely stated, "We are concerned now about performing silicone spacer surgery unilaterally, we have performed the procedure bilaterally on eight patients with bilateral superior oblique muscle overaction." This discussant agrees with the first part of this admonition, but disagrees with the second part. Bilateral tendon expanders for an Apattern strabismus with bilateral superior oblique overactions were justified only parenthetically in the presentation by noting that "no patient in this group was symptomatic," yet they acknowledged induced hypertropias in downgaze, unnoticed because such patients "usually have wellestablished suppression." There are several other wellestablished graded weakening procedures on the superior oblique for ?-pattern exotropias, such as a) excision of the posterior 3/4 of the superior oblique tendon at the insertion of the superior oblique, b) tenotomy, temporal to the superior rectus muscle, and c) tenotomy nasal to the superior rectus muscle. This discussant finds no rationale or supportive evidence for using tendon expanders in ?-pattern exotropias.

It has been this discussant's experience that repair of certain procedures such as a Jensen transposition procedure, and strabismus as a result of retinal detachment hardware in the orbit, are among the most difficult strabismus procedures to undo and correct. In both the cases reported by the authors the repairs resulted in free tenotomies of the superior obliques, plus additional surgeries with a yet incompletely resolved, induced defect in the important reading position. These procedures (including the tendon expander procedure) are unlike the usual recess or resect procedures wherein subsequent corrective procedures are usually restorative.

The authors refer extensively to the paper by the originator of the superior oblique spacer technique, Dr Kenneth Wright, so it is worthwhile to comment upon Wright's results and compare them with those of the present authors. Wright reported, "...of the four patients with Brown syndrome, three showed marked improvement of elevation in adduction, without consecutive superior oblique palsy." None of the four patients in the Wright series, nor in the present authors' series of two, had true Brown syndrome. I do not wish to deprecate one bit the attempt of Dr Wright and others to devise surgical procedures for a condition for which there is no uniformly satisfactory result. However, one must be very careful indeed not to transpose the indications and results of patients with Brown plus, ie, with primary position deviations and anomalous head position, with true Brown syndrome. Thus, one can not accept the statement that "results in patients with Brown syndrome were quite good" (Wright). Nor can one accept the present authors' conclusions that "the superior oblique tendon 'expander' procedure is now an established option in the surgical management of Brown syndrome or superior oblique muscle overaction." True Brown syndrome is not discussed by these authors. Nor can this discussant agree with the conclusion that "it is evidence from our reported cases that an overcorrection suggestive of a secondary superior oblique muscle palsy occurs in some cases." Rather, it is more likely that superior rectus contracture was the resultant complication.

Are there any indications for surgery for true Brown syndrome, ie, no vertical in any of the horizontal positions of gaze nor anomalous head positions? Historically, Harold W. Brown suggested a stretching or sheathectomy of the superior oblique that, at surgery, invariably produced a freed-up and normalized forced auction up and in. Alas, however, Brown syndrome reappeared the following day - and remained. This was followed by Dr Ed Dunlop's suggestion of continuing the forced duction daily - postoperatively. But, this too failed and was given up. Following Dr Dunlop's suggestion, I had a series of one patient many years ago in whom I freed up the ductions at surgery and, with a traction suture, held the eye in an up and in position for 2 weeks. With removal of the traction suture, the Brown syndrome did not reappear, but the eye remained up and in quite permanently. This series of one was, understandably, unpublished; but the experience was shared with colleagues. Following this, Drs Alan Scott and Philip Knapp published a series of patients on whom they sewed the eye up and in by a traction suture for a shorter period of time - and these results were published. In a recent personal communication, Dr Scott tells me that there was improvement in about 50% of the cases (1992). Let us not forget Dr Philip Knapp's "chicken suture" wherein he severed the tendon, allowed it to separate via a nonabsorbable suture that limited its separation (and allowed reconstruction and later identification if necessary). It appears that excessive hardware of any sort in the locale of the superior oblique sliding under the superior rectus muscle may have some complications in downgaze which this discussant believes to be due to restriction of superior rectus action; and we are appreciative to the authors of this paper for calling attention to them.

In true Brown syndrome there is no deviation in the primary position, nor in downgaze reading position. Any procedure that attempts to restore a rotation at the possible expense of these two important positions should be very carefully considered indeed. It appears, at the present time, there is no uniformly satisfactory procedure that seems to this discussant to be indicated for true Brown syndrome.

From The Smith-Kettlewell Eye Research Institute, San Francisco, Calif.

Reprint requests should be addressed to Arthur Jampolsky, MD, The Smith-Kettlewell Eye Research Institute, 2232 Webster St, San Francisco, CA 94 115.

FIGURE 4: Postoperative gaze measurements from case 1.At 4 and 12 weeks after placement of the 7-millimeter spacer, there are findings suggestive of a superior oblique muscle palsy, as well as a downgaze deficit. Jen weeks after removal of the silicone, and right inferior oblique recession 10.0 mm and left inferior rectus recession 3.0 mm, there is improvement of the right hypertropia. XT = exotropia; X = exophoria; LH = left hyperphoria; RH - right hyperphoria; RHT = right hypertropia; LHT = left hypertropia.

10.3928/0191-3913-19950101-08

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